RESUMO
Objective To eveluate the pancreatic injury induced by smoking alone or combined with alcohol consumption,and its possible mechanism.Methods The Wistar rats were divided into control group (n=10),smoking group (n=30),drinking group (n=42) and smoking combined with drinking group (combination group,n=48).Serum levels of interleukin (IL)-6,superoxide dismutase (SOD) activities,monocyte chemoattractant protein-1 (MCP-1) and hydroxyproline were determined at 4th-,8th- and 12th- week.The pathohistological changes of the pancreas were examined using HE staining and the expression of α-smooth muscle actin (α-SMA) were measured by immunohistochemistry.ResultsIn contrast to control group,pancreatic changes including cytoplasmic vacuolation and increased levels of α-SMA and hydroxyproline were found in both smoking and drinking groups at the 8th-week (P<0.01).Whereas these changes were aggravated in combination group (P<0.05).Serum level of IL-6 and MCP-1 expression in pancreatic tissue were significantly increased in smoking group when compared with control group.But MCP-1 expression was lower in drinking group than control group.Moreover,the SOD activity in pancreatic tissue decreased in smoking and drinking groups,especially in combination group.Conclusions Long-term smoking can induce cytoplasmic vacuolation in pancreatic acinar cells,enhance inflammatory factors and chemokine expression and aggravate oxidative stress response in pancreas.These changes are aggravated when smoking and drinking coexisted.The mechanism behind it may be associated with increased oxidative stress response in pancreas.